OBJECTIVE: The National Resident Matching Program (NRMP) is utilized by an increasing number of diagnostic radiology (DR) residents applying to subspecialty fellowships. Data characterizing Match outcomes based on program characteristics is limited. We sought to determine if fellowship or residency size, location, or perceived reputation was related with a program filling their quota. MATERIALS AND METHODS: Using public NRMP data from 2004-2022, DR residency, Breast Imaging (BI), Musculoskeletal (MSK), Interventional (IR), and Neuroradiology (NR) fellowship programs were characterized by geography, DR and fellowship quota, applicants per position (A/P), and reputation as determined by being an Aunt Minnie's Best DR Program Semifinalist, Doximity 2021-2022 Top 25, or US World News and Report (USWNR) Top Hospital. The DR program's reputation was substituted for fellowships at the same institution. A program was considered filled if it met quota. RESULTS: The 2022 A/P ratios were 1.02 (IR), 0.83 (BI), 0.75 (MSK), and 0.88 (NR). IR was excluded from additional analysis due to A/P >1. The combined BI, MSK, and NR fellowships filled 78% (529/679) positions and 56% (132/234) programs. Factors associated with higher program filling included: Doximity Top 25, Aunt Minnie Semifinalist, and Top 20 USWNR (p for all <0.001), DR residency quota >9 and fellowship quota >3 (p=<0.01). The Ohio Valley (Ohio, western Pennsylvania, West Virginia and Kentucky) filled the lowest at 39% of programs (p=0.06). CONCLUSION: Larger fellowship programs with a higher perceived reputation and larger underlying DR residency programs were significantly more likely to fill their NRMP quota.
Stuttering affects approximately 1 in 100 adults and can result in significant communication problems and social anxiety. It most often occurs as a developmental disorder but can also be caused by focal brain damage. These latter cases may lend unique insight into the brain regions causing stuttering. Here, we investigated the neuroanatomical substrate of stuttering using three independent datasets: (i) case reports from the published literature of acquired neurogenic stuttering following stroke (n = 20, 14 males/six females, 16-77 years); (ii) a clinical single study cohort with acquired neurogenic stuttering following stroke (n = 20, 13 males/seven females, 45-87 years); and (iii) adults with persistent developmental stuttering (n = 20, 14 males/six females, 18-43 years). We used the first two datasets and lesion network mapping to test whether lesions causing acquired stuttering map to a common brain network. We then used the third dataset to test whether this lesion-based network was relevant to developmental stuttering. In our literature dataset, we found that lesions causing stuttering occurred in multiple heterogeneous brain regions, but these lesion locations were all functionally connected to a common network centred around the left putamen, including the claustrum, amygdalostriatal transition area and other adjacent areas. This finding was shown to be specific for stuttering (PFWE < 0.05) and reproducible in our independent clinical cohort of patients with stroke-induced stuttering (PFWE < 0.05), resulting in a common acquired stuttering network across both stroke datasets. Within the common acquired stuttering network, we found a significant association between grey matter volume and stuttering impact for adults with persistent developmental stuttering in the left posteroventral putamen, extending into the adjacent claustrum and amygdalostriatal transition area (PFWE < 0.05). We conclude that lesions causing acquired neurogenic stuttering map to a common brain network, centred to the left putamen, claustrum and amygdalostriatal transition area. The association of this lesion-based network with symptom severity in developmental stuttering suggests a shared neuroanatomy across aetiologies.
Network neuroscience offers a unique framework to understand the organizational principles of the human brain. Despite recent progress, our understanding of how the brain is modulated by focal lesions remains incomplete. Resection of the temporal lobe is the most effective treatment to control seizures in pharmaco-resistant temporal lobe epilepsy (TLE), making this syndrome a powerful model to study lesional effects on network organization in young and middle-aged adults. Here, we assessed the downstream consequences of a focal lesion and its surgical resection on the brain's structural connectome, and explored how this reorganization relates to clinical variables at the individual patient level. We included adults with pharmaco-resistant TLE (n = 37) who underwent anterior temporal lobectomy between two imaging time points, as well as age- and sex-matched healthy controls who underwent comparable imaging (n = 31). Core to our analysis was the projection of high-dimensional structural connectome data-derived from diffusion MRI tractography from each subject-into lower-dimensional gradients. We then compared connectome gradients in patients relative to controls before surgery, tracked surgically-induced connectome reconfiguration from pre- to postoperative time points, and examined associations to patient-specific clinical and imaging phenotypes. Before surgery, individuals with TLE presented with marked connectome changes in bilateral temporo-parietal regions, reflecting an increased segregation of the ipsilateral anterior temporal lobe from the rest of the brain. Surgery-induced connectome reorganization was localized to this temporo-parietal subnetwork, but primarily involved postoperative integration of contralateral regions with the rest of the brain. Using a partial least-squares analysis, we uncovered a latent clinical-imaging signature underlying this pre- to postoperative connectome reorganization, showing that patients who displayed postoperative integration in bilateral fronto-occipital cortices also had greater preoperative ipsilateral hippocampal atrophy, lower seizure frequency, and secondarily generalized seizures. Our results bridge the effects of focal brain lesions and their surgical resections with large-scale network reorganization and inter-individual clinical variability, thus offering new avenues to examine the fundamental malleability of the human brain.
Recent epidemiological studies propose an association between parkinsonism and seizures, but the direction of this association is unclear. Focal brain lesions causing new-onset parkinsonism versus seizures may provide a unique perspective on the causal relationship between the two symptoms and involved brain networks. We studied lesions causing parkinsonism versus lesions causing seizures and utilized human connectome data to identify their connected brain networks. Brain networks for parkinsonism and seizures were compared using spatial correlations on a group and individual lesion level. Lesions not associated with either symptom were used as controls. Lesion locations from 29 patients with parkinsonism were connected to a brain network with the opposite spatial topography (spatial r =-0.85) compared to 347 patients with lesions causing seizures. A similar inverse relationship was found when comparing the connections that were most specific for lesions causing parkinsonism versus seizures on a group level (spatial r =- 0.51) and on an individual lesion level (average spatial r =-0.042; p<0.001). The substantia nigra was found to be most positively correlated to the parkinsonism network but most negatively correlated to the seizure network (spatial r >0.8). Brain lesions causing parkinsonism versus seizures map to opposite brain networks, providing neuroanatomical insight into conflicting epidemiological evidence.
OBJECTIVE: To determine if MRI altered management in patients ≥ 60 years old with chronic knee pain. MATERIALS AND METHODS: Consecutive patients ≥ 60 years old with knee MRI and radiographs within 90 days were included. Exclusion criteria included mass/malignancy, recent trauma, and infection. Standing AP and PA flexion views were evaluated using Kellgren-Lawrence (KL) and International Knee Documentation Committee (IKDC) scales. Pertinent clinical history was recorded. MRIs were considered to alter management if subchondral fracture was identified or subsequent arthroscopy was performed due to an MRI finding. RESULTS: Eighty-five knee MRI/radiograph exams were reviewed; mean 68.2 years (60-88), 47:38 F:M. Twenty knee MRIs (24%) had either a subchondral fracture (n = 9) or meniscal tear (n = 11) prompting arthroscopy. On PA flexion view, 0/20 of these studies had KL grade 4 and 70% (14/20) had KL grade 0-1 compared to the remaining MRIs having 15.4% (10/65) KL grade 4 and 38.5% (25/65) KL grade 0-1 (p = 0.03). A 10-pack-year tobacco history, 38% vs 18%, was associated with a subchondral fracture or arthroscopy (p = 0.06). Subchondral fractures were more prevalent in older patients (mean 72.4 vs 67.7 years; p = 0.03). CONCLUSION: In patients ≥ 60 years old with chronic knee pain, MRI altered management in ~ 24% of cases; 70% in patients with KL grade 0-1, and none in patients with KL grade 4. MRI may benefit older patients with minimal osteoarthritis but not those with end-stage disease. Patients with ≥ 10 pack years of smoking may also benefit from MRI.
Transcranial magnetic stimulation (TMS) and deep brain stimulation (DBS) can treat some neuropsychiatric disorders, but there is no consensus approach for identifying new targets. We localized causal circuit-based targets for anxiety that converged across multiple natural experiments. Lesions (n=451) and TMS sites (n=111) that modify anxiety mapped to a common normative brain circuit (r=0.68, p=0.01). In an independent dataset (n=300), individualized TMS site connectivity to this circuit predicted anxiety change (p=0.02). Subthalamic DBS sites overlapping the circuit caused more anxiety (n=74, p=0.006), thus demonstrating a network-level effect, as the circuit was derived without any subthalamic sites. The circuit was specific to trait versus state anxiety in datasets that measured both (p=0.003). Broadly, this illustrates a pathway for discovering novel circuit-based targets across neuropsychiatric disorders.
Neuromodulation trials for PTSD have yielded mixed results, and the optimal neuroanatomical target remains unclear. We analyzed three datasets to study brain circuitry causally linked to PTSD in military Veterans. After penetrating traumatic brain injury (n=193), lesions that reduced probability of PTSD were preferentially connected to a circuit including the medial prefrontal cortex (mPFC), amygdala, and anterolateral temporal lobe (cross-validation p=0.01). In Veterans without lesions (n=180), PTSD was specifically associated with connectivity within this circuit (p<0.01). Connectivity change within this circuit correlated with PTSD improvement after transcranial magnetic stimulation (TMS) (n=20) (p<0.01), even though the circuit was not directly targeted. Finally, we directly targeted this circuit with fMRI-guided accelerated TMS, leading to rapid resolution of symptoms in a patient with severe lifelong PTSD. All results were independent of depression severity. This lesion-based PTSD circuit may serve as a neuromodulation target for Veterans with PTSD.
Oculogyric crises are acute episodes of sustained, typically upward, conjugate deviation of the eyes. Oculogyric crises usually occur as the result of acute D2-dopamine receptor blockade, but the brain areas causally involved in generating this symptom remain elusive. Here, we used data from 14 previously reported cases of lesion-induced oculogyric crises and employed lesion network mapping to identify their shared connections throughout the brain. This analysis yielded a common network that included basal ganglia, thalamic, and brainstem nuclei, as well as the cerebellum. Comparison of this network with gene expression profiles associated with the dopamine system revealed spatial overlap specifically with the gene coding for dopamine receptor type 2 (DRD2) as defined by a large-scale transcriptomic database of the human brain. Furthermore, spatial overlap with DRD2 and DRD3 gene expression was specific to brain lesions associated with oculogyric crises when contrasted to lesions that led to other movement disorders. Our findings identify a common neural network causally involved in the occurrence of oculogyric crises and provide a pathophysiological link between lesion locations causing this syndrome and its most common pharmacological cause, namely DRD2 blockade.
The mouse retina contains over 40 types of retinal ganglion cells (RGCs) that differ in morphology, function, or gene expression. RGCs also differ by whether their axons target the brain.s ipsilateral or contralateral hemisphere. Contralaterally projecting RGCs (contraRGCs) are widespread in mouse retina, whereas ipsilateral projecting RGCs (ipsiRGCs) are confined to the ventro-temporal (VT) crescent of retina. In this study, we employed the Sert-Cre transgenic line, which had been reported to selectively label ipsiRGCs, to study ipsiRGCs during development. Although the number of Cre-expressing ipsiRGCs did not significantly increase with postnatal age, the region of retina that they occupied did, and by adulthood represented ~30% of the retinal surface. Unexpectedly, genetic ablation of Sert-Cre cells failed to fully disrupt ipsilateral projecting retinal axons, suggesting that not all ipsiRGCs generated Cre in Sert-Cre mice. To test this hypothesis, we retrogradely labeled ipsiRGCs in Sert-Cre mice which revealed that not all ipsiRGCs are labeled in Sert-Cre mice and a small population of contraRGCs flanking the VT crescent generates Cre in this line. These results do not negate the usefulness of the Sert-Cre mouse but do raise important caveats to the interpretation of such studies.
Retinal Ganglion Cells , Superior Colliculi , Animals , Mice , Superior Colliculi/anatomy & histology , Retina , Brain , Animals, Genetically Modified , Visual Pathways/anatomy & histology
OBJECTIVE: Patients with Alzheimer's disease (AD) have diffuse brain atrophy, but some regions, such as the anterior cingulate cortex (ACC), are spared and may even show increase in size compared to controls. The extent, clinical significance, and mechanisms associated with increased cortical thickness in AD remain unknown. Recent work suggested neural facilitation of regions anticorrelated to atrophied regions in frontotemporal dementia. Here, we aim to determine whether increased thickness occurs in sporadic AD, whether it relates to clinical symptoms, and whether it occur in brain regions functionally connected to-but anticorrelated with-locations of atrophy. METHODS: Cross-sectional clinical, neuropsychological, and neuroimaging data from the Alzheimer's Disease Neuroimaging Initiative were analyzed to investigate cortical thickness in AD subjects versus controls. Atrophy network mapping was used to identify brain regions functionally connected to locations of increased thickness and atrophy. RESULTS: AD patients showed increased thickness in the ACC in a region-of-interest analysis and the visual cortex in an exploratory analysis. Increased thickness in the left ACC was associated with preserved cognitive function, while increased thickness in the left visual cortex was associated with hallucinations. Finally, we found that locations of increased thickness were functionally connected to, but anticorrelated with, locations of brain atrophy (r = -0.81, p < 0.05). INTERPRETATION: Our results suggest that increased cortical thickness in Alzheimer's disease is relevant to AD symptoms and preferentially occur in brain regions functionally connected to, but anticorrelated with, areas of brain atrophy. Implications for models of compensatory neuroplasticity in response to neurodegeneration are discussed. ANN NEUROL 2024;95:929-940.
Alzheimer Disease , Atrophy , Magnetic Resonance Imaging , Humans , Alzheimer Disease/pathology , Alzheimer Disease/diagnostic imaging , Male , Female , Aged , Atrophy/pathology , Cross-Sectional Studies , Cerebral Cortex/pathology , Cerebral Cortex/diagnostic imaging , Aged, 80 and over , Gyrus Cinguli/pathology , Gyrus Cinguli/diagnostic imaging , Brain Cortical Thickness , Middle Aged
BACKGROUND: Disconjugate eye movements are essential for depth perception in frontal-eyed species, but their underlying neural substrates are largely unknown. Lesions in the midbrain can cause disconjugate eye movements. While vertically disconjugate eye movements have been linked to defective visuo-vestibular integration, the pathophysiology and neuroanatomy of horizontally disconjugate eye movements remains elusive. METHODS: A patient with a solitary focal midbrain lesion was examined using detailed clinical ocular motor assessments, binocular videooculography and diffusion-weighted MRI, which was co-registered to a high-resolution cytoarchitectonic MR-atlas. RESULTS: The patient exhibited both vertically and horizontally disconjugate eye alignment and nystagmus. Binocular videooculography showed a strong correlation of vertical and horizontal oscillations during fixation but not in darkness. Oscillation intensities and waveforms were modulated by fixation, illumination, and gaze position, suggesting shared visual- and vestibular-related mechanisms. The lesion was mapped to a functionally ill-defined area of the dorsal midbrain, adjacent to the posterior commissure and sparing nuclei with known roles in vertical gaze control. CONCLUSION: A circumscribed region in the dorsal midbrain appears to be a key node for disconjugate eye movements in both vertical and horizontal planes. Lesioning this area produces a unique ocular motor syndrome mirroring hallmarks of developmental strabismus and nystagmus. Further circuit-level studies could offer pivotal insights into shared pathomechanisms of acquired and developmental disorders affecting eye alignment.
Mesencephalon , Humans , Mesencephalon/diagnostic imaging , Mesencephalon/physiopathology , Mesencephalon/pathology , Male , Ocular Motility Disorders/physiopathology , Ocular Motility Disorders/etiology , Female , Eye Movements/physiology , Middle Aged , Nystagmus, Pathologic/physiopathology , Nystagmus, Pathologic/etiology , Nystagmus, Pathologic/diagnostic imaging , Adult
Retinal ganglion cell (RGC) axons provide direct input into several nuclei of the mouse visual thalamus, including the dorsal lateral geniculate nucleus (dLGN), which is important for classical image-forming vision, and the ventral lateral geniculate nucleus (vLGN), which is associated with non-image-forming vision. Through both activity- and morphogen-dependent mechanisms, retinal inputs play important roles in the development of dLGN, including the refinement of retinal projections, morphological development of thalamocortical relay cells (TRCs), the timing of corticogeniculate innervation, and the recruitment of inhibitory interneurons from progenitor zones. In contrast, little is known about the role of retinal inputs in the development of vLGN. Grossly, vLGN is divided into two domains, the retinorecipient external vLGN (vLGNe) and the non-retinorecipient internal vLGN (vLGNi). We previously found that vLGNe consists of transcriptionally distinct GABAergic subtypes that are distributed into at least four adjacent laminae. At present, it remains unclear whether retinal inputs influence the development of these cell-specific neuronal laminae in vLGNe. Here, we elucidated the developmental timeline for the formation and maintenance of these laminae in the mouse vLGNe and results indicate that these laminae are specified at or before birth, well before eye-opening and the emergence of experience-dependent visual activity. We observed that mutant mice without retinal inputs have a normal laminar distribution of GABAergic cells at birth; however, after the first week of postnatal development, these mutants exhibited a dramatic disruption in the laminar organization of inhibitory neurons and clear boundaries between vLGNe and vLGNi. Overall, our results show that while the formation of cell type-specific layers in vLGNe does not depend on RGC inputs, retinal signals are critical for their maintenance.
The Vietnam Head Injury Study has been curated by Dr Jordan Grafman since the 1980s in an effort to study patients with penetrating traumatic brain injuries suffered during the Vietnam War. Unlike many datasets of ischemic stroke lesions, the VHIS collected extraordinarily deep phenotyping and was able to sample lesion locations that are not constrained to typical vascular territories. For decades, this dataset has helped researchers draw causal links between neuroanatomical regions and neuropsychiatric symptoms. The value of the VHIS has only increased over time as techniques for analyzing the dataset have developed and evolved. Tools such as voxel lesion symptom mapping allowed one to relate symptoms to individual brain voxels. With the advent of the human connectome, tools such as lesion network mapping allow one to relate symptoms to connected brain networks by combining lesion datasets with new atlases of human brain connectivity. In a series of recent studies, lesion network mapping has been combined with the Vietnam Head Injury dataset to identify brain networks associated with spirituality, religiosity, consciousness, memory, emotion regulation, addiction, depression, and even transdiagnostic mental illness. These findings are enhancing our ability to make diagnoses, identify potential treatment targets for focal brain stimulation, and understand the human brain generally. Our techniques for studying brain lesions will continue to improve, as will our tools for modulating brain circuits. As these advances occur, the value of well characterized lesion datasets such as the Vietnam Head Injury Study will continue to grow. This study aims to review the history of the Vietnam Head Injury Study and contextualize its role in modern-day localization of neurological symptoms.
Brain Injuries, Traumatic , Connectome , Humans , Vietnam , Brain/pathology , Connectome/methods
BACKGROUND: The glenoid track concept for shoulder instability primarily describes the medial-lateral relationship between a Hill-Sachs lesion and the glenoid. However, the Hill-Sachs position in the craniocaudal dimension has not been thoroughly studied. HYPOTHESIS: Hill-Sachs lesions with greater inferior extension are associated with increased risk of recurrent instability after primary arthroscopic Bankart repair. STUDY DESIGN: Case-control study; Level of evidence, 3. METHODS: The authors performed a retrospective analysis of patients with on-track Hill-Sachs lesions who underwent primary arthroscopic Bankart repair (without remplissage) between 2007 and 2019 and had a minimum 2-year follow-up. Recurrent instability was defined as recurrent dislocation or subluxation after the index procedure. The craniocaudal position of the Hill-Sachs lesion was measured against the midhumeral axis on sagittal magnetic resonance imaging (MRI) using either a Hill-Sachs bisecting line through the humeral head center (sagittal midpoint angle [SMA], a measure of Hill-Sachs craniocaudal position) or a line tangent to the inferior Hill-Sachs edge (lower-edge angle [LEA], a measure of Hill-Sachs caudal extension). Univariate and multivariate regression were used to determine the predictive value of both SMA and LEA for recurrent instability. RESULTS: In total, 176 patients were included with a mean age of 20.6 years, mean follow-up of 5.9 years, and contact sport participation of 69.3%. Of these patients, 42 (23.9%) experienced recurrent instability (30 dislocations, 12 subluxations) at a mean time of 1.7 years after surgery. Recurrent instability was found to be significantly associated with LEA >90° (ie, Hill-Sachs lesions extending below the humeral head equator), with an OR of 3.29 (P = .022). SMA predicted recurrent instability to a lesser degree (OR, 2.22; P = .052). Post hoc evaluation demonstrated that LEA >90° predicted recurrent dislocations (subset of recurrent instability) with an OR of 4.80 (P = .003). LEA and SMA were found to be collinear with Hill-Sachs interval and distance to dislocation, suggesting that greater LEA and SMA proportionally reflect lesion severity in both the craniocaudal and medial-lateral dimensions. CONCLUSION: Inferior extension of an otherwise on-track Hill-Sachs lesion is a highly predictive risk factor for recurrent instability after primary arthroscopic Bankart repair. Evaluation of Hill-Sachs extension below the humeral equator (inferior equatorial extension) on sagittal MRI is a clinically facile screening tool for higher-risk lesions with subcritical glenoid bone loss. This threshold for critical humeral bone loss may inform surgical stratification for procedures such as remplissage or other approaches for at-risk on-track lesions.
Bankart Lesions , Joint Dislocations , Joint Instability , Shoulder Dislocation , Shoulder Joint , Humans , Young Adult , Adult , Shoulder Dislocation/diagnostic imaging , Shoulder Dislocation/surgery , Shoulder Dislocation/complications , Bankart Lesions/diagnostic imaging , Bankart Lesions/surgery , Bankart Lesions/complications , Shoulder Joint/diagnostic imaging , Shoulder Joint/surgery , Joint Instability/diagnostic imaging , Joint Instability/surgery , Joint Instability/etiology , Retrospective Studies , Case-Control Studies , Follow-Up Studies , Arthroscopy/methods , Humeral Head/diagnostic imaging , Humeral Head/surgery , Recurrence
Noninvasive brain stimulation technologies such as transcranial electrical and magnetic stimulation (tES and TMS) are emerging neuromodulation therapies that are being used to target the neural substrates of substance use disorders. By the end of 2022, 205 trials of tES or TMS in the treatment of substance use disorders had been published, with heterogeneous results, and there is still no consensus on the optimal target brain region. Recent work may help clarify where and how to apply stimulation, owing to expanding databases of neuroimaging studies, new systematic reviews, and improved methods for causal brain mapping. Whereas most previous clinical trials targeted the dorsolateral prefrontal cortex, accumulating data highlight the frontopolar cortex as a promising therapeutic target for transcranial brain stimulation in substance use disorders. This approach is supported by converging multimodal evidence, including lesion-based maps, functional MRI-based maps, tES studies, TMS studies, and dose-response relationships. This review highlights the importance of targeting the frontopolar area and tailoring the treatment according to interindividual variations in brain state and trait and electric field distribution patterns. This converging evidence supports the potential for treatment optimization through context, target, dose, and timing dimensions to improve clinical outcomes of transcranial brain stimulation in people with substance use disorders in future clinical trials.
Behavior, Addictive , Substance-Related Disorders , Humans , Transcranial Magnetic Stimulation/methods , Brain , Substance-Related Disorders/therapy , Prefrontal Cortex
OBJECTIVE: To determine the preferred ankle, knee, and elbow arthrography injection techniques for Society of Skeletal Radiology (SSR) members and whether more recently described techniques are gaining acceptance. We also sought to determine whether the concept of knowledge translation might explain differences between the preferred technique, year of fellowship graduation, and year the newer technique was described. MATERIALS AND METHODS: A 29-question survey was created in Qualtrics and submitted to current SSR members to determine if they perform knee, elbow, and ankle arthrography, and if so, the year of fellowship completion and preferred approaches. Survey respondents indicated the starting and ending needle tip positions for three knee, two elbow, and three ankle arthrography approaches using grids placed over provided frontal and lateral radiographs. RESULTS: Two hundred seventy-four SSR members (mean post-fellowship 13 years; range 0-38) completed the survey and performed fluoroscopic-guided knee (93%), elbow (95%), and ankle (75%) arthrography. Preferred approaches included the following: knee lateral subpatellar (43%), anterior (40%); elbow radiocapitellar (74%); ankle anterior/peritendon (70%), lateral mortise (24%). Preference of newer technique was related to fellowship graduation year and publication year for the ankle mortise (26% before, 42% after; p = 0.03) and posterior trans-triceps elbow articles (19% before, 33% after; p < 0.01). The anterior knee approach preference increased from 11% in 2008 to 40% (p ≤ 0.001). CONCLUSION: Nearly twice as many SSR members who graduated after the posterior trans-triceps and ankle mortise techniques were published prefer them for performing arthrography, possibly due to knowledge translation. The preference of the anterior knee arthrography approach has increased nearly fourfold since 2008.
Arthrography , Radiology , Humans , Arthrography/methods , Ankle , Elbow , Injections, Intra-Articular/methods
OBJECTIVE: Spontaneous confabulation is a symptom in which false memories are conveyed by the patient as true. The purpose of the study was to identify the neuroanatomical substrate of this complex symptom and evaluate the relationship to related symptoms, such as delusions and amnesia. METHODS: Twenty-five lesion locations associated with spontaneous confabulation were identified in a systematic literature search. The network of brain regions functionally connected to each lesion location was identified with a large connectome database (N=1,000) and compared with networks derived from lesions associated with nonspecific (i.e., variable) symptoms (N=135), delusions (N=32), or amnesia (N=53). RESULTS: Lesions associated with spontaneous confabulation occurred in multiple brain locations, but they were all part of a single functionally connected brain network. Specifically, 100% of lesions were connected to the mammillary bodies (familywise error rate [FWE]-corrected p<0.05). This connectivity was specific for lesions associated with confabulation compared with lesions associated with nonspecific symptoms or delusions (FWE-corrected p<0.05). Lesions associated with confabulation were more connected to the orbitofrontal cortex than those associated with amnesia (FWE-corrected p<0.05). CONCLUSIONS: Spontaneous confabulation maps to a common functionally connected brain network that partially overlaps, but is distinct from, networks associated with delusions or amnesia. These findings lend new insight into the neuroanatomical bases of spontaneous confabulation.
Connectome , Memory Disorders , Humans , Amnesia/diagnostic imaging , Brain/diagnostic imaging , Brain/pathology , Prefrontal Cortex/pathology , Datasets as Topic
Increasing evidence suggests that the clinical effects of transcranial magnetic stimulation are target dependent. Within any given symptom, precise targeting of specific brain circuits may improve clinical outcomes. This principle can also be extended across symptoms-stimulation of different circuits may lead to different symptom-level outcomes. This may include targeting different symptoms within the same disorder (such as dysphoria vs. anxiety in patients with major depression) or targeting the same symptom across different disorders (such as primary major depression and depression secondary to stroke, traumatic brain injury, epilepsy, multiple sclerosis, or Parkinson's disease). Some of these symptom-specific changes may be desirable, while others may be undesirable. This review focuses on the conceptual framework through which symptom-specific target circuits may be identified, tested, and implemented.
Depressive Disorder, Major , Parkinson Disease , Humans , Transcranial Magnetic Stimulation , Anxiety Disorders , Anxiety
